Highly branched phenotype of the petunia dad1-1 mutant is reversed by grafting
Highly branched phenotype of the petunia dad1-1 mutant is reversed by grafting
复制标题
DOI：
10.1104/pp.111.1.27
复制
发表时间：
1996-05-01
期刊：
影响因子：
7.4
通讯作者：
Napoli, C
中科院分区：
文献类型：
--
作者：
Napoli, C
隐性dad 1 -1等位基因的条件下，一个高度分支的生长习性，导致增殖的第一和第二阶分支。与野生型亲本不同，野生型亲本的侧向分枝延迟到子叶远端的第三或第四叶节，dad 1 -1从每个子叶腋开始侧向分枝。除了比野生型更快地开始侧向分枝外，dad 1 -1比野生型通过更多的主茎轴上的节点维持分枝。在保持与分支的倾向在基部节点，DAD 1 -1产生第二阶分支在最近端的节点上的第一阶分支和小芽从副芽在基部节点上的主芽轴。与突变相关的其他性状是开花晚、不定根形成、节间缩短和轻度叶片失绿。嫁接研究表明，一个dad 1 -1接穗，当嫁接到野生型股票，被转换成类似野生型的表型。此外，插入突变体砧木和突变体接穗之间的小的野生型中间砧片段足以将dad 1 -1接穗从突变体转化为接近野生型的外观。隐性dad 1 -1表型结合性状与细胞分裂素过度表达，生长素过度表达，和赤霉素的限制，这表明一个复杂的相互作用的激素在建立突变体表型。
The recessive dad1-1 allele conditions a highly branched growth habit resulting from a proliferation of first- and second-order branches. Unlike the wild-type parent, which has lateral branching delayed until the third or fourth leaf node distal to the cotyledons, dad1-1 initiates lateral branching from each cotyledon axil. In addition to initiating lateral branching sooner than the wild type, dad1-1 sustains branching through more nodes on the main shoot axis than the wild type. In keeping with a propensity for branching at basal nodes, dad1-1 produces second-order branches at the proximal-most nodes on first-order branches and small shoots from accessory buds at basal nodes on the main shoot axis. Additional traits associated with the mutation are late flowering, adventitious root formation, shortened internodes, and mild leaf chlorosis. Graft studies show that a dad1-1 scion, when grafted onto wild-type stock, is converted to a phenotype resembling the wild type. Furthermore, a small wild-type interstock fragment inserted between a mutant root stock and a mutant scion is sufficient to convert the dad1-1 scion from mutant to a near wild-type appearance. The recessive dad1-1 phenotype combines traits associated with cytokinin overexpression, auxin overexpression, and gibberellin limitation, which suggests a complex interaction of hormones in establishing the mutant phenotype.